Stavia posted the following on the thread I mentioned in the opening:
Stavia wrote:Bulldog, very good question
Here is an excerpt from UpToDate, the online medical textbook I subscribe to - short version is that is is not recommended to take an anti-inflammatory drug to reduce the risk of dementia at this stage. When we talk about inflammation we mean a broad sense of inflammation, which is caused by many different factors including diverse issues such as high blood sugars, micronutrient deficiency, poor diet, possibly gut barrier issues, obesity and many other subtle and interacting factors.NSAID therapy — Some epidemiologic studies, but not others, have suggested that nonsteroidal antiinflammatory drugs (NSAIDs) protect against the development of AD and cognitive decline [101-113], possibly by lowering levels of amyloidogenic Abeta42 protein [114-117]. Conflicting results regarding their efficacy may be due in part to the timing and duration of NSAID use, to differences in tracking NSAID use, and to the ApoE genotype status of the participants. Their use is not currently supported by randomized clinical trials.
The duration, dose, and timing of NSAID use may be important factors:
●A meta-analysis of cohort and case-control studies found a pooled relative risk (RR) of AD among NSAID users of 0.72 (95% CI 0.56-0.94); the RR among short, intermediate, and long-term users was 0.95 (CI 0.70-1.29), 0.83 (CI 0.65-1.06), and 0.27 (0.13-0.58) respectively . The RR among aspirin users was 0.87 (CI 0.70-1.07). In one of the larger observational studies, computerized pharmacy records of 6989 people aged >55 years found that long-term NASID use protected against the development of AD . With relative risk of AD of 0.95 in patients who had used NSAIDs for one month or less, 0.83 in patients who had used NSAIDs for more than one but less than 24 months, and 0.20 in patients who had used NSAIDs for 24 months or more.
●In the latter study, most of the NSAID effect in the long-term users was attributed to therapy two or more years before the onset of dementia, suggesting that there may be a critical period during which NSAID use is protective . This was also the finding of the Cache County, UT study in which NSAID use in midlife rather than late life was associated with less severe cognitive decline over eight years of follow-up .
●Another population-based cohort study found that heavy NSAID use in late life may be associated with an increased rather than decreased risk of AD (HR = 1.7) . In a subset of this cohort with autopsy data, the burden of neuritic plaque was associated a higher cumulative use of NSAIDs .
●No preferential benefit was found for those NSAIDS which are reported to selectively reduce Abeta42 (eg, ibuprofen, indomethacin, sulindac) compared with those which do not (eg, naproxen, etodolac), according to one large cohort study and the pooled results of six other cohort studies [111,120].
A large randomized trial studied the efficacy of naproxen, celecoxib, and placebo in the prevention of AD in 2528 individuals >70 years with a history of at least one family member with AD-like dementia . Imperfect screening had led to the enrollment of 53 persons with premorbid dementia or mild cognitive impairment. Analysis of the study population with these individuals excluded, after two years of follow-up, demonstrated that AD risk was actually increased in both active treatment groups (HR=4.1, 3.6). Other measures of cognition were not improved and were possibly worse in the treated groups . The trial was stopped early because of an increased risk of myocardial infarction in patients treated with naproxen . Long-term use of certain COX-2 inhibitor inhibitors has also been associated with an increased risk of cardiovascular events. (See "COX-2 selective inhibitors: Adverse cardiovascular effects".)
Another large, randomized study of 6377 participants found that older women randomly assigned to low dose aspirin had similar rates of cognitive decline compared to the placebo-treated group after more than 5 years of follow-up . Similarly, a 5-year study of low dose aspirin in 3350 individuals over 50 years found no effective of treatment on cognitive test scores .
Cyclooxygenase-2 (COX-2) inhibitors and NSAIDs should not be used for the treatment or prevention of dementia or cognitive impairment at this time.
Here is a fairly recent paper on acetaminophen:
Acetaminophen Inhibits Neuronal Inflammation and Protects Neurons from Oxidative Stress
"Background: Recent studies have demonstrated a link between the inflammatory response, increased cytokine formation, and neurodegeneration in the brain. The beneficial effects of anti-inflammatory drugs in neurodegenerative diseases, such as Alzheimer's disease (AD), have been documented. Increasing evidence suggests that acetaminophen has unappreciated anti-oxidant and anti-inflammatory properties. The objectives of this study are to determine the effects of acetaminophen on cultured brain neuronal survival and inflammatory factor expression when exposed to oxidative stress."
Any advice would be much appreciated!